Neuronal damage induced by perinatal asphyxia is attenuated by postinjury glutaredoxin-2 administration

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2017
Author
Romero, Juan Ignacio
Holubiec, Mariana Inés
Logica, Tamara
Rivière, Stéphanie
Hanschmann, Eva Maria
Kölliker Frers, Rodolfo
Tau, Julia
Blanco Calvo, Eduardo
Galeano, Pablo
Rodríguez de Fonseca, Fernando
Horst Lillig, Christopher
Capani, Francisco
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Romero, Juan Ignacio; Holubiec, Mariana Inés; Logica, Tamara; Rivière, Stéphanie; Hanschmann, Eva Maria; Kölliker Frers, Rodolfo; ... Capani, Francisco. (2017) . Neuronal damage induced by perinatal asphyxia is attenuated by postinjury glutaredoxin-2 administration. Oxidative Medicine And Cellular Longevity, 2017, vol. 2017, núm. 4162465, p. 1-14. https://doi.org/10.1155/2017/4162465.
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Abstract
The general disruption of redox signaling following an ischemia-reperfusion episode has been proposed as a crucial component in neuronal death and consequently brain damage. Thioredoxin (Trx) family proteins control redox reactions and ensure protein regulation via specific, oxidative posttranslational modifications as part of cellular signaling processes. Trx proteins function in the manifestation, progression, and recovery following hypoxic/ischemic damage. Here, we analyzed the neuroprotective effects of postinjury, exogenous administration of Grx2 and Trx1 in a neonatal hypoxia/ischemia model. P7 Sprague-Dawley rats were subjected to right common carotid ligation or sham surgery, followed by an exposure to nitrogen. 1 h later, animals were injected i.p. with saline solution, 10 mg/kg recombinant Grx2 or Trx1, and euthanized 72 h postinjury. Results showed that Grx2 administration, and to some extent Trx1, attenuated part of the neuronal damage associated with a perinatal hypoxic/ischemic damage, such as glutamate excitotoxicity, axonal integrity, and astrogliosis. Moreover, these treatments also prevented some of the consequences of the induced neural injury, such as the delay of neurobehavioral development. To our knowledge, this is the first study demonstrating neuroprotective effects of recombinant Trx proteins on the outcome of neonatal hypoxia/ischemia, implying clinical potential as neuroprotective agents that might counteract neonatal hypoxia/ischemia injury.
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http://hdl.handle.net/10459.1/60425
DOI
https://doi.org/10.1155/2017/4162465
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Oxidative Medicine And Cellular Longevity, 2017, vol. 2017, núm. 4162465, p. 1-14
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cc-by (c) Romero, Juan Ignacio et al., 2017
Except where otherwise noted, this item's license is described as cc-by (c) Romero, Juan Ignacio et al., 2017